摘要
42只新西兰幼兔,随机分为对照、窒息、窒息+SOD及窒息+尼莫地平4组。各组动物均于实验开始后24h心脏取血测OFR,测脑组织水含量,并观察脑病理改变。窒息组织与对照组比较,血清LPO、脑水含量明显增高,血中SOD,GSH-Px活力明显降低,脑病理改变明显,且窒息组LPO与脑水含量呈正相关关系。两用药组与窒息组相比,血清LPO、脑水含量明显减少,SOD、GSH-Px活力明显增高,脑病理改变减轻。提示OFR参与了窒息所致脑损伤的病理过程,外源性SOD和尼莫地平对窒息幼兔脑组织有保护作用。
young rabbits were divided into four different groups, which werecontrol,asphyxial, asphyxia treated with SOD,asphyxia treated with nimodipine. Bloodwere drawn from the heart of all animals 24 hours after the start of experiment.Theblood were tested for OFR,H_2O content of cerebral tissue and pathological changes ofcerebral tissue were also observed.We compared asphyxial with control group and foundthat in aspyxial group serum LPO and H_2O of cerebral tissue were increased markedly,while blood SOD and GSH-Px decreased significantly.Pathologic changes in the brainwere obvious and serum LPO was in a positive correlation with H_2O content of cerebraltissue. Compared two treated groups with asphyxial group,serum LPO and cerebral H_2Oof the treated groups decreased significantly, while SOD and GSH-Px increased significantly,and pathologic changes in brain were relieyed.It was concluded that OFR induced damagein brain subjected to acute asphyxia. Foreign SOD and nimodipine effectively prcventeddamage of the brain tissue of young rabbit.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1994年第5期537-540,共4页
Chinese Journal of Pathophysiology
关键词
窒息
脑损伤
氧自由基
钙通道阻滞剂
SOD
Asphyxia,brain damage
Oxygen free radicals(OFR)
Calcium channed blockers